APL Bioengineering最新文献_第9页

Survivin as a mediator of stiffness-induced cell cycle progression and proliferation of vascular smooth muscle cells. Survivin作为僵硬诱导细胞周期进展和血管平滑肌细胞增殖的介质。

IF 6 3区医学

APL Bioengineering Pub Date : 2023-10-30 eCollection Date: 2023-12-01 DOI: 10.1063/5.0150532

John C Biber, Andra Sullivan, Joseph A Brazzo, Yuna Heo, Bat-Ider Tumenbayar, Amanda Krajnik, Kerry E Poppenberg, Vincent M Tutino, Su-Jin Heo, John Kolega, Kwonmoo Lee, Yongho Bae

{"title":"Survivin as a mediator of stiffness-induced cell cycle progression and proliferation of vascular smooth muscle cells.","authors":"John C Biber, Andra Sullivan, Joseph A Brazzo, Yuna Heo, Bat-Ider Tumenbayar, Amanda Krajnik, Kerry E Poppenberg, Vincent M Tutino, Su-Jin Heo, John Kolega, Kwonmoo Lee, Yongho Bae","doi":"10.1063/5.0150532","DOIUrl":"10.1063/5.0150532","url":null,"abstract":"Stiffened arteries are a pathology of atherosclerosis, hypertension, and coronary artery disease and a key risk factor for cardiovascular disease events. The increased stiffness of arteries triggers a phenotypic switch, hypermigration, and hyperproliferation of vascular smooth muscle cells (VSMCs), leading to neointimal hyperplasia and accelerated neointima formation. However, the mechanism underlying this trigger remains unknown. Our analyses of whole-transcriptome microarray data from mouse VSMCs cultured on stiff hydrogels simulating arterial pathology identified 623 genes that were significantly and differentially expressed (360 upregulated and 263 downregulated) relative to expression in VSMCs cultured on soft hydrogels. Functional enrichment and gene network analyses revealed that these stiffness-sensitive genes are linked to cell cycle progression and proliferation. Importantly, we found that survivin, an inhibitor of apoptosis protein, mediates stiffness-dependent cell cycle progression and proliferation as determined by gene network and pathway analyses, RT-qPCR, immunoblotting, and cell proliferation assays. Furthermore, we found that inhibition of cell cycle progression did not reduce survivin expression, suggesting that survivin functions as an upstream regulator of cell cycle progression and proliferation in response to ECM stiffness. Mechanistically, we found that the stiffness signal is mechanotransduced via the FAK-E2F1 signaling axis to regulate survivin expression, establishing a regulatory pathway for how the stiffness of the cellular microenvironment affects VSMC behaviors. Overall, our findings indicate that survivin is necessary for VSMC cycling and proliferation and plays a role in regulating stiffness-responsive phenotypes.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 4","pages":"046108"},"PeriodicalIF":6.0,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10618027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71427789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Investigations on artificially extending the spectral range of natural vision. 人工扩大自然视觉光谱范围的研究。

IF 6 3区医学

APL Bioengineering Pub Date : 2023-10-24 eCollection Date: 2023-12-01 DOI: 10.1063/5.0156463

Abhijith Krishnan, C S Deepak, K S Narayan

引用次数: 0

Survivin regulates intracellular stiffness and extracellular matrix production in vascular smooth muscle cells. Survivin调节血管平滑肌细胞的细胞内硬度和细胞外基质的产生。

IF 6 3区医学

APL Bioengineering Pub Date : 2023-10-20 eCollection Date: 2023-12-01 DOI: 10.1063/5.0157549

Amanda Krajnik, Erik Nimmer, Joseph A Brazzo, John C Biber, Rhonda Drewes, Bat-Ider Tumenbayar, Andra Sullivan, Khanh Pham, Alanna Krug, Yuna Heo, John Kolega, Su-Jin Heo, Kwonmoo Lee, Brian R Weil, Deok-Ho Kim, Sachin A Gupte, Yongho Bae

{"title":"Survivin regulates intracellular stiffness and extracellular matrix production in vascular smooth muscle cells.","authors":"Amanda Krajnik, Erik Nimmer, Joseph A Brazzo, John C Biber, Rhonda Drewes, Bat-Ider Tumenbayar, Andra Sullivan, Khanh Pham, Alanna Krug, Yuna Heo, John Kolega, Su-Jin Heo, Kwonmoo Lee, Brian R Weil, Deok-Ho Kim, Sachin A Gupte, Yongho Bae","doi":"10.1063/5.0157549","DOIUrl":"10.1063/5.0157549","url":null,"abstract":"Vascular dysfunction is a common cause of cardiovascular diseases characterized by the narrowing and stiffening of arteries, such as atherosclerosis, restenosis, and hypertension. Arterial narrowing results from the aberrant proliferation of vascular smooth muscle cells (VSMCs) and their increased synthesis and deposition of extracellular matrix (ECM) proteins. These, in turn, are modulated by arterial stiffness, but the mechanism for this is not fully understood. We found that survivin is an important regulator of stiffness-mediated ECM synthesis and intracellular stiffness in VSMCs. Whole-transcriptome analysis and cell culture experiments showed that survivin expression is upregulated in injured femoral arteries in mice and in human VSMCs cultured on stiff fibronectin-coated hydrogels. Suppressed expression of survivin in human VSMCs significantly decreased the stiffness-mediated expression of ECM components related to arterial stiffening, such as collagen-I, fibronectin, and lysyl oxidase. By contrast, expression of these ECM proteins was rescued by ectopic expression of survivin in human VSMCs cultured on soft hydrogels. Interestingly, atomic force microscopy analysis showed that suppressed or ectopic expression of survivin decreases or increases intracellular stiffness, respectively. Furthermore, we observed that inhibiting Rac and Rho reduces survivin expression, elucidating a mechanical pathway connecting intracellular tension, mediated by Rac and Rho, to survivin induction. Finally, we found that survivin inhibition decreases FAK phosphorylation, indicating that survivin-dependent intracellular tension feeds back to maintain signaling through FAK. These findings suggest a novel mechanism by which survivin potentially modulates arterial stiffness.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 4","pages":"046104"},"PeriodicalIF":6.0,"publicationDate":"2023-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10590228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49692949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PCSK9 activation promotes early atherosclerosis in a vascular microphysiological system. PCSK9激活促进血管微物理系统中的早期动脉粥样硬化。

IF 6.6 3区医学

APL Bioengineering Pub Date : 2023-10-16 eCollection Date: 2023-12-01 DOI: 10.1063/5.0167440

Jounghyun H Lee, Kevin L Shores, Jason J Breithaupt, Caleb S Lee, Daniella M Fodera, Jennifer B Kwon, Adarsh R Ettyreddy, Kristin M Myers, Benny J Evison, Alexandra K Suchowerska, Charles A Gersbach, Kam W Leong, George A Truskey

{"title":"PCSK9 activation promotes early atherosclerosis in a vascular microphysiological system.","authors":"Jounghyun H Lee, Kevin L Shores, Jason J Breithaupt, Caleb S Lee, Daniella M Fodera, Jennifer B Kwon, Adarsh R Ettyreddy, Kristin M Myers, Benny J Evison, Alexandra K Suchowerska, Charles A Gersbach, Kam W Leong, George A Truskey","doi":"10.1063/5.0167440","DOIUrl":"10.1063/5.0167440","url":null,"abstract":"Atherosclerosis is a primary precursor of cardiovascular disease (CVD), the leading cause of death worldwide. While proprotein convertase subtilisin/kexin 9 (PCSK9) contributes to CVD by degrading low-density lipoprotein receptors (LDLR) and altering lipid metabolism, PCSK9 also influences vascular inflammation, further promoting atherosclerosis. Here, we utilized a vascular microphysiological system to test the effect of PCSK9 activation or repression on the initiation of atherosclerosis and to screen the efficacy of a small molecule PCSK9 inhibitor. We have generated PCSK9 over-expressed (P+) or repressed (P-) human induced pluripotent stem cells (iPSCs) and further differentiated them to smooth muscle cells (viSMCs) or endothelial cells (viECs). Tissue-engineered blood vessels (TEBVs) made from P+ viSMCs and viECs resulted in increased monocyte adhesion compared to the wild type (WT) or P- equivalents when treated with enzyme-modified LDL (eLDL) and TNF-α. We also found significant viEC dysfunction, such as increased secretion of VCAM-1, TNF-α, and IL-6, in P+ viECs treated with eLDL and TNF-α. A small molecule compound, NYX-1492, that was originally designed to block PCSK9 binding with the LDLR was tested in TEBVs to determine its effect on lowering PCSK9-induced inflammation. The compound reduced monocyte adhesion in P+ TEBVs with evidence of lowering secretion of VCAM-1 and TNF-α. These results suggest that PCSK9 inhibition may decrease vascular inflammation in addition to lowering plasma LDL levels, enhancing its anti-atherosclerotic effects, particularly in patients with elevated chronic inflammation.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 4","pages":"046103"},"PeriodicalIF":6.6,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10581720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49683473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A tissue-engineered model of the atherosclerotic plaque cap: Toward understanding the role of microcalcifications in plaque rupture. 动脉粥样硬化斑块帽的组织工程模型：了解微钙化在斑块破裂中的作用。

IF 6.6 3区医学

APL Bioengineering Pub Date : 2023-09-29 eCollection Date: 2023-09-01 DOI: 10.1063/5.0168087

Imke Jansen, Hanneke Crielaard, Tamar Wissing, Carlijn Bouten, Frank Gijsen, Ali C Akyildiz, Eric Farrell, Kim van der Heiden

{"title":"A tissue-engineered model of the atherosclerotic plaque cap: Toward understanding the role of microcalcifications in plaque rupture.","authors":"Imke Jansen, Hanneke Crielaard, Tamar Wissing, Carlijn Bouten, Frank Gijsen, Ali C Akyildiz, Eric Farrell, Kim van der Heiden","doi":"10.1063/5.0168087","DOIUrl":"10.1063/5.0168087","url":null,"abstract":"Rupture of the cap of an atherosclerotic plaque can lead to thrombotic cardiovascular events. It has been suggested, through computational models, that the presence of microcalcifications in the atherosclerotic cap can increase the risk of cap rupture. However, the experimental confirmation of this hypothesis is still lacking. In this study, we have developed a novel tissue-engineered model to mimic the atherosclerotic fibrous cap with microcalcifications and assess the impact of microcalcifications on cap mechanics. First, human carotid plaque caps were analyzed to determine the distribution, size, and density of microcalcifications in real cap tissue. Hydroxyapatite particles with features similar to real cap microcalcifications were used as microcalcification mimics. Injected clusters of hydroxyapatite particles were embedded in a fibrin gel seeded with human myofibroblasts which deposited a native-like collagenous matrix around the particles, during the 21-day culture period. Second harmonic multiphoton microscopy imaging revealed higher local collagen fiber dispersion in regions of hydroxyapatite clusters. Tissue-engineered caps with hydroxyapatite particles demonstrated lower stiffness and ultimate tensile stress than the control group samples under uniaxial tensile loading, suggesting increased rupture risk in atherosclerotic plaques with microcalcifications. This model supports previous computational findings regarding a detrimental role for microcalcifications in cap rupture risk and can further be deployed to elucidate tissue mechanics in pathologies with calcifying soft tissues.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 3","pages":"036120"},"PeriodicalIF":6.6,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41172465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In vivo laser speckle contrast imaging of 4-aminopyridine- or pentylenetetrazole-induced seizures. 4-氨基吡啶或戊四唑诱导癫痫发作的体内激光斑点对比成像。

IF 6 3区医学

APL Bioengineering Pub Date : 2023-09-28 eCollection Date: 2023-09-01 DOI: 10.1063/5.0158791

Yuhling Wang, Vassiliy Tsytsarev, Lun-De Liao

{"title":"In vivo laser speckle contrast imaging of 4-aminopyridine- or pentylenetetrazole-induced seizures.","authors":"Yuhling Wang, Vassiliy Tsytsarev, Lun-De Liao","doi":"10.1063/5.0158791","DOIUrl":"https://doi.org/10.1063/5.0158791","url":null,"abstract":"Clinical and preclinical studies on epileptic seizures are closely linked to the study of neurovascular coupling. Obtaining reliable information about cerebral blood flow (CBF) in the area of epileptic activity through minimally invasive techniques is crucial for research in this field. In our studies, we used laser speckle contrast imaging (LSCI) to gather information about the local blood circulation in the area of epileptic activity. We used two models of epileptic seizures: one based on 4-aminopyridine (4-AP) and another based on pentylenetetrazole (PTZ). We verified the duration of an epileptic seizure using electrocorticography (ECoG). We applied the antiepileptic drug topiramate (TPM) to both models, but its effect was different in each case. However, in both models, TPM had an effect on neurovascular coupling in the area of epileptic activity, as shown by both LSCI and ECoG data. We demonstrated that TPM significantly reduced the amplitude of 4-AP-induced epileptic seizures (4-AP+TPM: 0.61 ± 0.13 mV vs 4-AP: 1.08 ± 0.19 mV; p < 0.05), and it also reduced gamma power in ECoG in PTZ-induced epileptic seizures (PTZ+TPM: 38.5% ± 11.9% of the peak value vs PTZ: 59.2% ± 3.0% of peak value; p < 0.05). We also captured the pattern of CBF changes during focal epileptic seizures induced by 4-AP. Our data confirm that the system of simultaneous cortical LSCI and registration of ECoG makes it possible to evaluate the effectiveness of pharmacological agents in various types of epileptic seizures in in vivo models and provides spatial and temporal information on the process of ictogenesis.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 3","pages":"036119"},"PeriodicalIF":6.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41143283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Current state of the art and future directions for implantable sensors in medical technology: Clinical needs and engineering challenges. 医疗技术中植入式传感器的现状和未来方向：临床需求和工程挑战。

IF 6 3区医学

APL Bioengineering Pub Date : 2023-09-27 eCollection Date: 2023-09-01 DOI: 10.1063/5.0152290

David Yogev, Tomer Goldberg, Amir Arami, Shai Tejman-Yarden, Thomas E Winkler, Ben M Maoz

{"title":"Current state of the art and future directions for implantable sensors in medical technology: Clinical needs and engineering challenges.","authors":"David Yogev, Tomer Goldberg, Amir Arami, Shai Tejman-Yarden, Thomas E Winkler, Ben M Maoz","doi":"10.1063/5.0152290","DOIUrl":"https://doi.org/10.1063/5.0152290","url":null,"abstract":"Implantable sensors have revolutionized the way we monitor biophysical and biochemical parameters by enabling real-time closed-loop intervention or therapy. These technologies align with the new era of healthcare known as healthcare 5.0, which encompasses smart disease control and detection, virtual care, intelligent health management, smart monitoring, and decision-making. This review explores the diverse biomedical applications of implantable temperature, mechanical, electrophysiological, optical, and electrochemical sensors. We delve into the engineering principles that serve as the foundation for their development. We also address the challenges faced by researchers and designers in bridging the gap between implantable sensor research and their clinical adoption by emphasizing the importance of careful consideration of clinical requirements and engineering challenges. We highlight the need for future research to explore issues such as long-term performance, biocompatibility, and power sources, as well as the potential for implantable sensors to transform healthcare across multiple disciplines. It is evident that implantable sensors have immense potential in the field of medical technology. However, the gap between research and clinical adoption remains wide, and there are still major obstacles to overcome before they can become a widely adopted part of medical practice.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 3","pages":"031506"},"PeriodicalIF":6.0,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10539032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41120073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phenotyping neuroblastoma cells through intelligent scrutiny of stain-free biomarkers in holographic flow cytometry. 通过全息流式细胞术中无染色生物标志物的智能检测对神经母细胞瘤细胞进行表型分析。

IF 6 3区医学

APL Bioengineering Pub Date : 2023-09-21 eCollection Date: 2023-09-01 DOI: 10.1063/5.0159399

Daniele Pirone, Annalaura Montella, Daniele Sirico, Martina Mugnano, Danila Del Giudice, Ivana Kurelac, Matilde Tirelli, Achille Iolascon, Vittorio Bianco, Pasquale Memmolo, Mario Capasso, Lisa Miccio, Pietro Ferraro

{"title":"Phenotyping neuroblastoma cells through intelligent scrutiny of stain-free biomarkers in holographic flow cytometry.","authors":"Daniele Pirone, Annalaura Montella, Daniele Sirico, Martina Mugnano, Danila Del Giudice, Ivana Kurelac, Matilde Tirelli, Achille Iolascon, Vittorio Bianco, Pasquale Memmolo, Mario Capasso, Lisa Miccio, Pietro Ferraro","doi":"10.1063/5.0159399","DOIUrl":"https://doi.org/10.1063/5.0159399","url":null,"abstract":"To efficiently tackle certain tumor types, finding new biomarkers for rapid and complete phenotyping of cancer cells is highly demanded. This is especially the case for the most common pediatric solid tumor of the sympathetic nervous system, namely, neuroblastoma (NB). Liquid biopsy is in principle a very promising tool for this purpose, but usually enrichment and isolation of circulating tumor cells in such patients remain difficult due to the unavailability of universal NB cell-specific surface markers. Here, we show that rapid screening and phenotyping of NB cells through stain-free biomarkers supported by artificial intelligence is a viable route for liquid biopsy. We demonstrate the concept through a flow cytometry based on label-free holographic quantitative phase-contrast microscopy empowered by machine learning. In detail, we exploit a hierarchical decision scheme where at first level NB cells are classified from monocytes with 97.9% accuracy. Then we demonstrate that different phenotypes are discriminated within NB class. Indeed, for each cell classified as NB its belonging to one of four NB sub-populations (i.e., CHP212, SKNBE2, SHSY5Y, and SKNSH) is evaluated thus achieving accuracy in the range 73.6%-89.1%. The achieved results solve the realistic problem related to the identification circulating tumor cell, i.e., the possibility to recognize and detect tumor cells morphologically similar to blood cells, which is the core issue in liquid biopsy based on stain-free microscopy. The presented approach operates at lab-on-chip scale and emulates real-world scenarios, thus representing a future route for liquid biopsy by exploiting intelligent biomedical imaging.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 3","pages":"036118"},"PeriodicalIF":6.0,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10519746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41171275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Generation of direct current electrical fields as regenerative therapy for spinal cord injury: A review. 直流电场的产生作为脊髓损伤的再生疗法：综述。

IF 6.6 3区医学

APL Bioengineering Pub Date : 2023-09-19 eCollection Date: 2023-09-01 DOI: 10.1063/5.0152669

Lukas Matter, Bruce Harland, Brad Raos, Darren Svirskis, Maria Asplund

引用次数: 0

Magnetic force-based cell manipulation for in vitro tissue engineering. 用于体外组织工程的基于磁力的细胞操作。

IF 6 3区医学

APL Bioengineering Pub Date : 2023-09-19 eCollection Date: 2023-09-01 DOI: 10.1063/5.0138732

Huiqian Hu, L Krishaa, Eliza Li Shan Fong

{"title":"Magnetic force-based cell manipulation for in vitro tissue engineering.","authors":"Huiqian Hu, L Krishaa, Eliza Li Shan Fong","doi":"10.1063/5.0138732","DOIUrl":"10.1063/5.0138732","url":null,"abstract":"Cell manipulation techniques such as those based on three-dimensional (3D) bioprinting and microfluidic systems have recently been developed to reconstruct complex 3D tissue structures in vitro. Compared to these technologies, magnetic force-based cell manipulation is a simpler, scaffold- and label-free method that minimally affects cell viability and can rapidly manipulate cells into 3D tissue constructs. As such, there is increasing interest in leveraging this technology for cell assembly in tissue engineering. Cell manipulation using magnetic forces primarily involves two key approaches. The first method, positive magnetophoresis, uses magnetic nanoparticles (MNPs) which are either attached to the cell surface or integrated within the cell. These MNPs enable the deliberate positioning of cells into designated configurations when an external magnetic field is applied. The second method, known as negative magnetophoresis, manipulates diamagnetic entities, such as cells, in a paramagnetic environment using an external magnetic field. Unlike the first method, this technique does not require the use of MNPs for cell manipulation. Instead, it leverages the magnetic field and the motion of paramagnetic agents like paramagnetic salts (Gadobutrol, MnCl2, etc.) to propel cells toward the field minimum, resulting in the assembly of cells into the desired geometrical arrangement. In this Review, we will first describe the major approaches used to assemble cells in vitro-3D bioprinting and microfluidics-based platforms-and then discuss the use of magnetic forces for cell manipulation. Finally, we will highlight recent research in which these magnetic force-based approaches have been applied and outline challenges to mature this technology for in vitro tissue engineering.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"7 3","pages":"031504"},"PeriodicalIF":6.0,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10511261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41172466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0